Anal fistula : the diagnosis and treatment.2014.pdf

Herand Abcarian
Editor

Anal Fistula
Principles and
Management

123


Anal Fistula



Herand Abcarian
Editor

Anal Fistula
Principles and Management


Editor
Herand Abcarian, M.D., F.A.C.S.
Professor of Surgery
The University of Illinois at Chicago
Chairman, Division of Colon and Rectal Surgery
John Stroger Hospital of Cook Country
Chicago, IL, USA

ISBN 978-1-4614-9013-5
ISBN 978-1-4614-9014-2 (eBook)

DOI 10.1007/978-1-4614-9014-2
Springer New York Heidelberg Dordrecht London
Library of Congress Control Number: 2013953886
© Springer Science+Business Media New York 2014
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For Karen



Foreword

Anal abscess and fistula have been a scourge of civilization for centuries. Hippocrates offered
a treatise on fistula in ancient Greece. In the 1300s John of Arderne, considered by many to be
the father of modern British surgery, was notorious for his successful treatment of fistulas in
Knights of the Round Table. King Louis XIV of France suffered from a famous chronic fistula
that gave rise to the use of a cutting seton in the1600s. Frederick Salmon in 1854 opened in
downtown London the St. Mark’s Hospital for Fistula and other Diseases of the Rectum. This
institution is considered to be the birthplace of modern colon and rectal surgery. To this institution Dr. Joseph Mathews traveled to study anal surgery and returned to Louisville, Kentucky,
to establish the first Department of Proctology in the United States, applying the knowledge
gained at St. Mark’s. Dr. Mathews was the first American surgeon to limit his practice to anorectal surgery and went on to become a founder of the American Proctologic Association (the
precursor of the American Society of Colon and Rectal Surgeons) and its first president.
Consistent among these historical developments is the clinicopathologic entity of anal fistula.
Despite the relatively high frequency of this disease, treatment remains controversial primarily because of the risk of incontinence after surgery. As a result, alternate operative procedures and other palliative adjuncts that control infection without sacrificing muscle continue to
evolve. Increasingly sophisticated diagnostic evaluation and imaging studies have resulted in
an increasing array of possible treatments, including in some instances a return to more basic
fistula operations.
This volume on anal fistula is, to my knowledge, the most recent and comprehensive reference for this disease, including even a discussion of the use of stem cells. The contributors are
all experienced clinicians; this lends immeasurable credibility to each of their chapters. Of
equal or greater importance is the experience and expertise of the editor. As a result, we are
presented with an invaluable resource to assist in the diagnosis and treatment of a historically
challenging problem.
Boston, MA, USA

David J. Schoetz Jr., M.D.

vii



Preface

It is almost 2 decades since the publication of the last book dedicated solely to fistula in ano by
Phillips and Lunniss [1]. Since then the readers interested in management of fistula in ano have
had to search the textbooks of Surgery and Colon and Rectal Surgery for relevant information.
The need for a more recent book dedicated to fistula in ano arises from the proliferation of
sphincter sparing procedures which have dominated the colon and rectal surgery literature
since the mid 1990s.
This volume represents a compilation of many chapters dealing with alternatives in sphincter sparing surgery as well as traditional fistulotomy. In addition, basic topics such as applied
anatomy, relationship of anorectal abscess and fistulas, clinical assessment, and current imaging modalities have been covered. The most recent developments include the use of adiposederived stem cells in the treatment of anal fistula, video-assisted anal fistula treatment
(VAAFT), and ligation of intersphincteric fistula tract (LIFT).
In addition to incidence and prevalence, causes of operative failures, fistula surgery in the
era of evidence-based medicine, as well as alternative approaches to fistulas which recur
despite all therapeutic measures are also addressed in this volume.
It is impossible to have a multi-author book and not have any redundancy among chapters.
However, the repetition if any, within the context of the covered topics, in my opinion, is a plus
rather than a distraction.
It is my hope that this volume will be a useful companion for the interested surgeon and will
be a source of reference for many alternative treatments of this frustrating disease.
Chicago, IL, USA

Herand Abcarian, M.D., F.A.C.S.

Reference
Phillips RK, Lunniss PJ, editors. Anal fistula: surgical evaluation and management. London: Hodder
Education; 1995.

ix



Contents

1

Epidemiology, Incidence and Prevalence of Fistula in Ano .................................
Richard L. Nelson and Herand Abcarian

1

2

Applied Anatomy .....................................................................................................
Russell K. Pearl

5

3

Relationship of Abscess to Fistula ..........................................................................
Herand Abcarian

13

4

Classification and Treatment of Anorectal Infections ..........................................
Adrian E. Ortega and Kyle G. Cologne

17

5

Clinical Assessment of Anal Fistulas ......................................................................
Herand Abcarian

27

6

Clinical Assessment and Imaging Modalities of Fistula in Ano ..........................
Kyle G. Cologne, Juan Antonio Villanueva-Herrero,
Enrique Montaño-Torres, and Adrian E. Ortega

31

7

Classification and Management Strategies ............................................................
Herand Abcarian

39

8

Seton (Loose, Cutting, Chemical) ...........................................................................
Vamsi R. Velchuru

45

9

Fistulotomy and Lay Open Technique ...................................................................
Philip Tozer and Robin K.S. Phillips

53

10

Fistulectomy with Primary Sphincter Reconstruction .........................................
Alexander Herold

65

11

Fibrin Sealant ...........................................................................................................
José R. Cintron

69

12

Biologic Fistula Plugs...............................................................................................
Samuel Eisenstein and Alex Jenny Ky

83

13

Synthetic Fistula Plug ..............................................................................................
Alex Jenny Ky, Michael Polcino, and Alero T. Nanna

89

14

Endorectal Advancement Flap ...............................................................................
Christine C. Jensen

97

15

Dermal Advancement Flap ..................................................................................... 109
Christine C. Jensen

16

Ligation of Intersphincteric Fistula Tract (LIFT) ................................................ 115
Ariane M. Abcarian

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xii

Contents

17

Video-Assisted Anal Fistula Treatment (VAAFT)................................................. 121

Piercarlo Meinero and Lorenzo Mori

18

Stem Cell Application in Fistula Disease ............................................................... 129
Damian Garcia-Olmo and Hector Guadalajara-Labajo

19

Crohn’s Disease ........................................................................................................ 139
James Fleshman and Rachel Tay

20

Tuberculosis Fistulas................................................................................................ 159
Pravin Jaiprakash Gupta

21

Fistula Surgery in the Era of Evidence-Based Medicine ...................................... 171
Richard L. Nelson and Herand Abcarian

22

Causes of Operative Failure .................................................................................... 177
Mohammad Ali Abbass and Maher Aref Abbas

23

Recurrence/Persistence After Fistula Treatment: What Next? ........................... 191

Herand Abcarian

Index .................................................................................................................................. 195


Contributors

Herand Abcarian, M.D., F.A.C.S. The University of Illinois at Chicago, Division of Colon
and Rectal Surgery, John Stroger Hospital of Cook Country, IL, USA
Maher Aref Abbass, M.D., F.A.C.S., F.A.S.C.R.S. Department of Surgery, Kaiser
Permanente, Los Angeles, CA, USA
Center for Minimally Invasive Surgery, Los Angeles Medical Center, Los Angeles, CA, USA
Mohammad Ali Abbas, M.D. Department of Surgery, Kaiser Permanente, Los Angeles
Medical Center, Los Angeles, CA, USA
Ariane M. Abcarian, M.D. Department of Surgery, University of Minnesota, Chicago,
MN, USA
José R. Cintron, M.D., F.A.C.S., F.A.S.C.R.S. Division of Colon and Rectal Surgery, John
H. Stroger Jr. Hospital of Cook County, Chicago, IL, USA
Kyle G. Cologne, M.D. Clinic Tower, Los Angeles, CA, USA
Samuel Eisenstein, M.D. Department of Surgery, Mount Sinai School of Medicine,
New York, NY, USA
James Fleshman, M.D., F.A.C.S., F.A.S.C.R.S. Department of Surgery, Baylor University
Medical Center, Dallas, TX, USA
Ross Fraser, C.I.S.S.P., I.S.S.A.P. Sextant Corporation, Toronto, ON, Canada
Damian Garcia-Olmo, M.D., Ph.D. Colorectal Surgery Unit, La Paz University Hospital,
Universidad Autonoma de Madrid, Madrid, Spain
Hector Guadalajara-Labajo, M.D. Colorectal Surgery Unit, La Paz University Hospital,
Universidad Autonoma de Madrid, Madrid, Spain
Alexander Herold, M.D., Ph.D. Deutches End-und Dickdarm-Zentrum Mannheim,
Mannheim, Germany

Pravin Jaiprakash Gupta, MS, F.I.C.A., F.I.C.S., F.A.I.S., F.A.S.C.R.S. Fine Morning
Hospital and Research Center, Nagpur, India
Christine C. Jensen, M.D., M.P.H. Department of Surgery, University of Minnesota,
St. Paul, MN, USA
Alex Jenny Ky, B.A., M.D. Department of Surgery, Mount Sinai School of Medicine,
New York, NY, USA
Piercarlo Meinero, M.D. Department of General Surgery, Sestri Levante Hospital, ASL 4
Chiavarese, Sestri Levante, Genova, Italy
Enrique Montaño-Torres, M.D. Clinica Especializada en Colon, Recto y Ano (CECRA)
and Hospital General Regional de Iztapalapa, Mexico DF, Mexico

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xiv

Lorenzo Mori, M.D. Department of General Surgery, Sestri Levante Hospital, ASL 4
Chiavarese, Sestri Levante, Genova, Italy
Alero T. Nanna, B.S., M.D. Department of Surgery, Mount Sinai School of Medicine,
New York, NY, USA
Richard L. Nelson, M.D., F.A.C.S. Northern General Hospital, Herr Road Sheffield, South
Yorkshire, UK
Adrian E. Ortega, M.D. Clinic Tower, Los Angeles, CA, USA
Russell K. Pearl, M.D., M.S. (Surg.) Division of Colon and Rectal Surgery, University of
Illinois at Chicago, Chicago, IL, USA
Robin K.S. Phillips, M.B.B.S., M.S., F.R.C.S. St. Mark’s Hospital, London, UK
Michael Polcino, M.D. Department of Surgery, Mount Sinai Hospital, New York, NY, USA
Rachel Tay, M.D. Department of Surgery, Baylor University Medical Center, Dallas,
TX, USA
Philip Tozer, M.B.B.S., M.D. (Res.), M.R.C.S., M.C.E.M. St. Mark’s Fistula Research Unit,

St. Mark’s Hospital, London, UK
Vamsi R. Velchuru, M.B.B.S., F.R.C.S. (Edin.), F.R.C.S. (Gen. Surg.) Department of
General Surgery, James Paget University Hospitals Foundation Trust, Yarmouth, Norfolk, UK
Juan Antonio Villanueva-Herrero, M.D. Clinica Especializada en Colon Recto y Ano
(Cecra) and Hospital General de Mexico, Mexico City, Mexico

Contributors


1

Epidemiology, Incidence
and Prevalence of Fistula in Ano
Richard L. Nelson and Herand Abcarian

Incidence
Anorectal fistulas have been the subject of medical and lay
literature for over 2,500 years. The term fistula is ascribed to
John Arderne (1307–1392) whose classic work on anal fistula is still in print. However, it is important to note that in
Ayurvedic medicine, Suhruta (b ~800 bc) described both fistulotomy and fistulectomy as well as the chemical seton
using Kshara Sutra [1]. Hippocrates (b ~460 bc) described
the use of horsehair (seta) in the treatment of anal fistulas.
Fistulas have been written about in many languages and geographical locations throughout the years [2–4]. The true incidence of anal fistulas is unknown.
Most publications on anal fistula reflect the authors’ experience, some quite large, from a single institution [4–6]. This,
however, does not address the incidence of the disease due to
the lack of proper denominator. Also it is difficult, if not
impossible, to accurately assess the incidence of anorectal
abscess because so many drain spontaneously or are incised
and drained in a surgeon’s office, emergency department or
surgicenter. On the other hand, hospital discharges or formal

operations in the operation rooms are usually recorded and
are available for statistical evaluation. Thus among the 1,000
patients presented to the Surgical Section of the Diagnostic
Clinic at the University of Virginia, 150 had anorectal pathology, 4 (0.4 %) had an abscess and 8 (0.8 %) had fistula. This
is quite comparable to 532 fistulas treated in a population of
77,372 patients admitted to Brooklyn Hospital between 1930
and 1939 for an incidence of 0.69 % [7]. Also Buie reported

an incidence of 5 % anal fistulas in patients with anorectal
abscesses seen at the Mayo Clinic [8].
Using operating room data in Helsinki Finland (1969–1978),
the incidence of fistulas was calculated to be 8.6 per 100,000
populations (males 12.3 %, females 5.6 %). Nelson in his
meta-analysis equated this with 20,000–25,000 fistulas
treated annually in the US [9]. Interestingly, the ambulatory
case of the National Center for Health Statistics reported
24,000 patients with a primary diagnosis of fistula treated in
US Hospitals in 1979. This number has decreased drastically
to 3,800 in 1999 possibly due to more and more ambulatory
approaches [9].
The incidence of anorectal fistula can be estimated from the
number of anorectal abscesses. In a series reported by
Ramanujam from a large inner city hospital, the incidence of
fistula was 34 % [4]. This is almost identical to another US
study [10] and a Canadian study [11] both reporting from single
institutions. Calculating backward, this would translate to an
estimated annual incidence of 68,000–96,000 cases in the US [9].

Etiology
Fistulas in the overwhelming majority of cases arise from

prior abscesses. Other causes such as hemorrhoidectomy,
foreign body perforation, and trauma are of less frequency.
Inflammatory bowel disease, more commonly Crohn’s disease, has been known to be associated with anorectal fistulas.
Specific diseases such as tuberculosis and actinomycosis are
much less frequent in the Western world. Tubercular fistulas are
covered in a separate section. The origin of anal abscess and
the relationship of abscesses to fistulas is covered in Chap. 3.

R.L. Nelson, M.D., F.A.C.S.
Northern General Hospital, Herr Road Sheffield, South Yorkshire,
S5 7AU, UK

Age and Sex

H. Abcarian, M.D., F.A.C.S. (*)
The University of Illinois at Chicago, Division of Colon and Rectal
Surgery, John Stroger Hospital of Cook Country, IL 60612, USA
e-mail:

Data on age and sex can be extracted from single series.
Most patients with anal fistula are between the ages of 20 and
60 with mean age of 40 in both genders. In the Sainio report,

H. Abcarian (ed.), Anal Fistula: Principles and Management, DOI 10.1007/978-1-4614-9014-2_1,
© Springer Science+Business Media New York 2014

1


2

men were afflicted twice as frequently as women (12.3 % vs.
5.6 %) [5]. In two large series reported from Cook County
Hospital in Chicago, the male to female ratio was also 2:1 [4, 12].
Hill reported treating 636 patients of whom nine were less
than 9 years old and were all boys [13]. Similarly, Mazier
reported 1,000 cases of fistula treated at the Ferguson Clinic
of whom 25 were younger than 10 years of age and nine of
the ten were boys [14]. Piazza and Radhakrishnan reported
anorectal abscesses in the pediatric population. Of 40
patients, 33 were boys and seven girls. Twenty-one were
younger than 2 years old, 20 were less than 9 months of age
and all were boys [15].
Rosen and colleagues reported 18 infants who were
treated with incision and drainage of abscess and expectant
therapy of established fistulas. In 18 of 18 patients (100 %),
the fistula resolved without the need for surgery [16]. This
might reinforce the concept put forward by Fitzgerald et al.
that fistulas in childhood are of congenital etiology [17].

Race
There are few epidemiologic studies regarding racial distribution of fistulas. In the series reported by Read and Abcarian
[12], 92 % of the patients were African American which
closely corresponded to the racial makeup of that particular
inner city hospital population. However, the patients were
younger with a peak incidence in ages 20–29 years and 61 %
were between the ages of 15–29 [12].

Seasonal Occurrence
No seasonal variation has been found in incidence of abscess

fistulas, although the study by Vasilavsky and Gordon
reported the higher incidence in June and lowest in the
months of August and September in Montreal, Canada [11].

Personal Hygiene and Sedentary Occupation
Although both implicated, personal hygiene and sedentary
lifestyle have not been shown to have a statistical significance [12].

Bowel Habits
Vasilavsky and Gordon reported that of 103 patients, diarrhea was the presenting symptom in 7 % [11]. However in
most published series in adults, diarrhea or constipation was
infrequently seen to be significant risk for fistulas [14].

R.L. Nelson and H. Abcarian

Risk of Cancer
Long-standing chronic draining wounds predispose to
development of cancer. Such is also the case of anal fistulas
[18, 19]. Nelson and colleagues reported six cancers in
chronic fistulas which on the average were present for
13.8 years [20, 21]. None of the six cancers had an intraluminal component and were not suspected preoperatively.
Several case-control and cohort studies have also shown an
association between intractable fistulas and development of
cancer [22]. In cases where cancers develop in a clinically
preexisting fistula, it is easy to blame the fistula as a contributing factor. Adenocarcinoma of the anal canal is an
aggressive disease [23]. The pathology of cancer in chronic
inflammation has been well documented in diseases such as
ulcerative colitis [24]. Because chronic inflammation due
to anal fistulas can be easily treated operatively with low
morbidity (in contrast to restorative proctocolectomy and

ileal pouch anal anastomosis in chronic ulcerative colitis),
it stands to reason that anal fistulas should be treated surgically and expeditiously soon after diagnosis.

Conclusion
Although the etiology of abscess fistulas is clear and less
controversial, the exact incidence and prevalence of fistulas
is not known due to poor data available from outpatient
treatment centers. The disease predominates in adults with a
male to female ratio of 2:1. The rare but potentially lethal
development of cancer in long-standing fistulas mandates
early treatment of this disease soon after diagnosis.

References
1. Sankaran PS. Sushruta’s contribution to surgery. Varanasi:
Ideological Book House; 1976.
2. Akinola DO, Hamed AD. Fistula in ano in Nigerians. Trop
Gastroenterol. 1989;10:153–7.
3. Navruzov SN, Dul’tsev IV, Salamov KN. Causes and prevention of
rectal fistula recurrences. Vestn Khir Im I I Grek. 1981;27:43–6.
4. Ramanujam PS, Prasad ML, Abcarian H, Tan AB. Perianal abscess
and fistulas; a study of 1023 patients. Dis Colon Rectum. 1984;27:
593–7.
5. Sainio P. Fistula in ano in a defined population. Incidence and
epidemiologic aspects. Ann Chir Gynaecol. 1984;73:219–24.
6. Shrum RC. Anorectal pathology in 1000 consecutive patients with
suspected surgical disorders. Dis Colon Rectum. 1959;2:469–72.
7. Buda AM. General candidates of fistula in ano: the role of foreign
bodies as causative factors fistulas. Am J Surg. 1941;54:384–7.
8. Buie SL. Sr practice proctology. 2nd ed. Springfield, IL: Charles C
Thomas; 1960.

9. Nelson RL. Anorectal Abscess fistulas. What do we know? Surg
Clin North Am. 2002;82:1139–51.


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Epidemiology, Incidence and Prevalence of Fistula in Ano

10. Scoma JA, Salvati EP, Rubin RJ. Incidence of fistulas subsequent to
anal abscesses. Dis Colon Rectum. 1974;17(3):357–9.
11. Vasilevsky CA, Gordon PH. The incidence of recurrent abscesses
or fistula-in-ano following anorectal suppuration. Dis Colon
Rectum. 1984;27(2):126–30.
12. Read DR, Abcarian H. A prospective survey of 474 patients with
anorectal abscess. Dis Colon Rectum. 1979;22(8):566–8.
13. Hill JR. Fistulas and fistulous abscesses in the anorectal region:
personal experience in management. Dis Colon Rectum. 1967;
10(6):421–34.
14. Mazier WP. The treatment and care of anal fistulas: a study of 1,000
patients. Dis Colon Rectum. 1971;14(2):134–44.
15. Piazza DJ, Radhakrishnan J. Perianal abscess and fistula-in-ano in
children. Dis Colon Rectum. 1990;33(12):1014–6.
16. Rosen NG, Gibbs DL, Soffer SZ, Hong A, Sher M, Pena A. The nonoperative treatment of fistula in ano. J Pediatr Surg. 2000;35:938–9.

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17. Fitzgerald RJ, Harding B, Ryan W. Fistula in ano in childhood:
a congenital etiology. J Pediatr Surg. 1985;20:80–1.
18. Corman BC. All’s well that ends well Shakespeare’s treatment of
anal fistula. Dis Colon Rectum. 1998;41:914–24.
19. Abcarian H. Anorectal infections: abscess-fistula. Clin Colon

Rectal Surg. 2011;24:14–21.
20. Nelson RL, Malik A. Anorectal fistula. Sheffield: Northern General
Hospital; 2010.
21. Nelson RL, Prasad ML, Abcarian H. Anal carcinoma presenting as
a perirectal abscess or fistula. Arch Surg. 1985;120:632–5.
22. Nelson RL, Abcarian H. Do hemorrhoids cure cancer? Sem Colon
Rectal Surg. 1996;6:178–81.
23. Tarazi R, Nelson RL. Adenocarcinoma of the anus. Sem Colon
Rectal Surg. 1995;6:169–73.
24. Shacter E, Weitzman SA. Chronic inflammation and cancer.
Oncology. 2002;16:217–36.


2

Applied Anatomy
Russell K. Pearl

Introduction
A thorough understanding of anorectal anatomy is essential
for the surgeon treating a patient with an anorectal fistula.
Proper surgical decision-making mandates intimate knowledge of factors such as the architecture of the sphincter muscles, the distribution of anal glands, and the geography of the
anorectal spaces. This chapter begins with a brief overview
of current concepts of anorectal anatomy with emphasis on
structures contributing to the etiology and surgical management of fistulas. It is followed by a discussion of practical
guidelines such as operative recommendations as to the
amount of sphincter that can be divided safely at one setting,
when to use marking or dividing setons, tips to avoid nerve
injury, and the anatomic reasons why certain treatment
options fail.

Overview of Pelvic Floor and Anorectal
Anatomy
The Pelvic Floor
The pelvic floor is formed by overlapping paired musculotendinous sheets of predominantly striated fibers known as
the levator ani muscles (Fig. 2.1). The major components of
this pelvic diaphragm are the pubococcygeus and the iliococcygeus muscles, although the posteriorly situated coccygeus
muscles are sometimes included in this group. Recent evidence suggests that the puborectalis sling, which functions to

R.K. Pearl, M.D., M.S. (Surg.) (*)
Division of Colon and Rectal Surgery, University of Illinois
at Chicago, 840 S. Wood Street, 518E CSB, MC 958, Chicago,
IL 60612, USA
e-mail:

angulate the anorectal junction anteriorly, is actually an integral
part of both the levator ani and external anal sphincter
complexes [1]. The levator ani is innervated from branches
of the fourth sacral nerves on its pelvic surface and by the
perineal branch of the pudendal nerve on its underside.
The puborectalis receives additional innervation from below
through the inferior rectal nerves.
The pubococcygeus originates from the posterior inferior
aspect of the pubis and the inner anterior surface of the obturator fascia, including a portion of the arcus tendineus of the
levator ani. Its anterior fibers insert medially into the central
tendon of the perineum (hiatal ligament), where they fuse
with the musculature of the prostate, vagina, and perineal
body to form the levator prostate, pubovaginalis, and pubourethralis muscles. Some of these intermediate fibers also
travel caudally along the intersphincteric plane and contribute
to the conjoined longitudinal coat of the anal canal. The muscular fibers of the pubococcygeus merge posteriorly into

the broad fibrous band that inserts into the anococcygeal
ligament, anterior sacrococcygeal ligament, and coccyx.
The iliococcygeus arises from the arcus tendineus of the
fascia of the internal obturator muscle posterior and caudal
to the origin of the pubococcygeus. The fibers run posteromedially, where they merge and insert into the anococcygeal
ligament and the last two segments of sacrum.
The puborectalis is the most caudal and controversial
component of the levator ani complex. It arises from the
posterior aspects of the body of the pubis, the inferior pubic
ramis, the superior fascia of the urogenital diaphragm, and
the adjacent obturator internus fascia and loops around the
rectum to form a strong U-shaped sling. Medial fibers of
the puborectalis fan out and insert into the central tendon of
the perineum where they intermingle with fibers from the
pubococcygeus and contribute to the conjoined longitudinal
muscle of the anal canal. The puborectalis sling, together
with the upper borders of the internal and external sphincters, forms the anorectal ring, which delineates the surgical
anal canal from the rectum.

H. Abcarian (ed.), Anal Fistula: Principles and Management, DOI 10.1007/978-1-4614-9014-2_2,
© Springer Science+Business Media New York 2014

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6

R.K. Pearl

Fig. 2.1 Overview of the pelvic

floor muscles and anal sphincters
seen from below

Fig. 2.2 Coronal view of the anal canal, lower rectum, and surrounding spaces. The enlarged view on the right highlights the architecture of the
sphincter muscles and anal glands

Rectum and Anal Canal
The rectum begins at the level of the third sacral vertebra and
in general follows along the curvature of the sacrum and coccyx for its entire length of 12–15 cm (Fig. 2.2). In addition,
it has three lateral curves; the upper and lower ones are convex to the right, the middle one convex to the left. The inner
aspects of these three transverse infoldings correspond to the
rectal valves of Houston. At the rectosigmoid junction, the
fibers of the taenia spread out to form the longitudinal muscle layer of the rectum, which surrounds the inner circular

muscle layer. The outer muscle coat is slightly thicker on the
anterior and posterior rectal walls than on its lateral surfaces,
contributing to the formation of three lateral curves.
The upper surface of the rectum is covered by the peritoneum on its anterior and lateral surfaces. The middle third
is covered on its anterior surface only, and the lower third is
entirely below the peritoneal reflection. The middle valve
of Houston is approximately at the level of the anterior peritoneal reflection.
The posterior wall of the rectum is covered with a thick
layer of pelvic fascia (fascia propria). A strong sheet of


2

Applied Anatomy

fascia (Waldeyer’s or rectosacral fascia) arises from the

fourth sacral segment, tracks forward and downward, and
attaches to the fascia propria on the posterior surface of the
rectal wall at the anorectal junction. The lower portion of the
rectum is supported on each side by reflections of endopelvic
fascia known as the lateral stalks of the rectum. The anterior
extraperitoneal surface of the rectum is covered by
Denonvilliers’ visceral pelvic fascia which extends to the
urogenital diaphragm running between the rectum and prostate or vagina.
As the rectum passes through the pelvic diaphragm at the
level of the anorectal ring, it changes its name, shape, and
direction. The anal canal begins at this point and extends for
approximately 4 cm to the anal verge (surgical anal canal).
The circular lumen of the rectum flattens into an anteroposterior slit because of its attachment to the perineal body and
coccyx along with the medial pressure exerted by the ischiorectal fat pads. The puborectalis sling in its normal contracted
state angulates the anorectal junction forward to create an 80°
bend, the perineal flexure, which may assist the external
sphincter mechanism in maintaining fecal continence.
The internal sphincter is a continuation of the involuntary
layer of circular smooth muscle of the rectum that begins at
the level of the anorectal ring. As it proceeds distally, it
becomes appreciably thicker, and its rounded lower margin
can usually be palpated about 1–2 cm below the dentate line.
The internal sphincter, like the puborectalis, is tonically contracted “at rest”.
The conjoined longitudinal muscle coat that surrounds
the internal sphincter arises from medial fibers of the pubococcygeus and puborectalis. These striated voluntary fibers
course along the intersphincteric plane, fan out through the
subcutaneous portion of the external sphincter, and attach to
the anoderm and perianal skin, constituting the corrugator
cutis ani muscle.
Several versions of the musculature of the external sphincter

have been proposed, ranging from the single continuous muscle sheet model of Goligher to the three distinct loop theory of
Shafik [2, 3]. The inconsistencies of these various descriptions
are most likely based on differences in age, sex, and individual
variation among the subjects, as well as on differences in points
of orientation among investigators (anatomists, physiologists,
radiologists, clinical surgeons). For example, a clinical surgeon
repairing a sphincter injury with an overlapping sphincteroplasty generally does not appreciate several subdivisions of
the external sphincter. In addition, the external sphincter
complex acts as a single functional unit, as demonstrated by
electromyography. More recently anal sphincter anatomy
has been investigated by high-spatial-resolution endoanal
MR imaging [4]. These findings will be discussed in more
detail later in this chapter.
Perhaps all that can be stated definitively with respect to
structure is that the external anal sphincter is an elliptical

7

cylinder of striated muscle that surrounds the anal canal, and
at least the large central portion (superficial component) is
firmly tethered to the coccyx, forming the anococcygeal
ligament.
Of particular interest is the composition of the fibers of
the external sphincter. It is made up of two different types
of striated muscle, type I and type II which function independently, even though they are fully integrated with each other.
The type I muscle fibers, although voluntary in appearance,
behave as involuntary smooth muscle by maintaining a state
of tonic contraction in much of the same manner as the internal sphincter. The type II muscle mass is capable of powerful
contractions far exceeding the baseline level of the type I
fibers. However, these type II fibers can only maintain this

maximal level of contraction for a short time before they
become fatigued.
The mucosa of the upper portion of the anal canal is lined
primarily by columnar epithelium. The lower portion or anatomic anal canal extends from the dentate line to the anal
verge and is lined with anoderm, a thin layer of stratified
squamous epithelium that lacks sweat glands and hair follicles. Interspersed between the mucosa of the proximal anal
canal and the serrated margin of the dentate line is a narrow
indistinct band of cuboidal epithelium known as the transitional zone, which represents the embryological remnants of
the cloacal membrane.
Several longitudinal mucosal folds, the columns of
Morgagni, arise in the proximal anal canal and terminate at the
dentate line, where they surround the anal crypts. The majority
of the branched tubular anal glands that originate from the
depths of these crypts are located in the posterior quadrant of
the anal canal, and will be discussed in more detail later.
In addition, the normally pink mucosa of the upper anal canal
appears purple where it overlies the three vascular anal cushions often referred to as the internal hemorrhoids.
The mucosa proximal to the dentate line lacks somatic
innervation. In contrast, the anoderm is richly endowed with
cutaneous sensory nerve endings. The blood supply to the
rectum and anal canal originates at three levels (Fig. 2.3).
The superior rectal artery, the principal blood supply to the
upper and middle portion of the rectum, begins as the terminal branch of the inferior mesenteric artery, where it crosses
over the left common iliac vessels. As it descends within the
sigmoid mesocolon, it bifurcates at the level of the third
sacral vertebra into right and left branches that course along
and within either side of the rectal wall. Each vessel divides
further so that an average of five small mucosal arteries
terminate at the level of the anal valves. There appears to be
a paucity of anastomoses on the anterior and posterior

surfaces of the rectum between the two collateral branches
of the superior rectal artery.
The middle rectal arteries usually arise from the internal
iliac arteries, travel along the anterolateral surface of the


8

R.K. Pearl

Fig. 2.3 The blood supply and venous drainage of the rectum and anal
canal. The arrows indicate the direction of lymphatic drainage

Fig. 2.4 Lateral view of the rectum and anal canal illustrating the
course and distribution of the pelvic autonomic nerves. Note the proximity of the pelvic plexus to the lower third of the rectum

lower rectum, traversing Denonvilliers’ fascia, and enter the
rectal wall at the level of the anorectal ring. Although the
middle rectal arteries do not run within the lateral stalks,
accessory branches may occasionally be found coursing
through these ligaments.
The inferior rectal arteries enter the posterolateral aspects
of the isciorectal fossae as offshoots of the internal pudendal
arteries, which run in Alcock’s canals. Each of these arteries
divides further into two to four vessels that supply the external and internal sphincter, as well as the lining of the anal
canal.
Although the degree of confluence between the vessels
supplying the rectum and anal canal is controversial, it
appears that all three vascular systems are interconnected by
a rich intramural plexus. The contribution of the middle

sacral artery to this network is at best small and variable.
The venous drainage of the rectum and anal canal parallels the arterial supply. Therefore, blood from the rectum and
upper part of the anal canal returns through the superior
rectal vein into the portal system, whereas the middle and
inferior rectal veins empty into the caval circulation.
The submucosal veins of the distal anal canal do not have a
special connection with the portal circulation. Contrary to

earlier beliefs, there is no significant increase in the incidence of symptomatic hemorrhoids in patients with portal
hypertension.
The lymphatic system of rectum and anal canal follows
the course of the regional blood supply. Lymphatic drainage
from the anal canal proximal to the dentate line courses
cephalad along the superior rectal vessels and laterally by
way of the middle rectal lymphatics to the internal iliac
nodes. Lymph from the anal canal below the dentate line
usually drains to the inguinal lymph nodes.
The rectum, upper portion of the anal canal, bladder, and
genitals are innervated by fibers of the autonomic nervous
system (Fig. 2.4). The external sphincter and anoderm are
supplied by somatic nerves.
The sympathetic nerves to these pelvic structures originate from the lower thoracic and upper lumbar spinal segments as preganglionic sympathetic fibers that synapse with
postganglionic fibers in the preaortic plexus and lumbar
sympathetic chains. They then course the pelvis adjacent to
the ilicac vessels, ureters, and lateral pelvic wall. The preaortic plexus is adherent to the anterior wall of the aorta and the
common iliac arteries. The lumbar sympathetic chains pass
underneath the common iliac vessels and join the fibers from


2

Applied Anatomy

the preaortic plexus to form the left and right hypogastric
plexuses just distal to the bifurcation of the aorta. These
plexuses are covered by pelvic peritoneum and are generally
adherent to the posterolateral pelvic walls.
Preganglionic parasympathetic nerves that arise from the
second, third, and fourth sacral segments (nervi erigentes)
descend into the pelvis and intermingle with the sympathetic
fibers from the hypogastric nerves to form the pelvic plexuses [5]. The pelvic plexuses are at the level of the lower
third of the rectum just above the levator ani muscles and are
situated well lateral to the pararectal reflections of the endopelvic fascia known as the lateral stalks of the rectum. This
dense reticulum of sympathetic and parasympathetic nerves
continues anterolaterally around the bladder and into the
prostate and penis.
Sensation to the perianal region and anal canal distal to
the dentate line is conveyed by afferent fibers of the inferior
rectal nerves. The mucosa of the rectum and proximal anal
canal lacks somatic sensory innervation so that mucosa
injury caused by biopsy, cauterization, polypectomy, or rubber bands ligation is not perceived as painful. The dull, aching sensation sometimes experienced in this region during
transanal procedures is probably mediated via the pelvic
parasympathetic nerves.

Anatomic Considerations Relating to Fistula
Surgery: Anal Glands
Situated within the 4–12 pockets or anal crypts found at the
dentate line are the openings to a variable number of straight
and branched anal glands (Fig. 2.2) [6]. These glands are
lined with stratified squamous epithelium and were first

described by Chiari in 1878. More than one gland may open
into the same crypt, while half the crypts have no communication with the gland. These tubular glands extend into the
submucosa in a downward and outward direction with twothirds of them entering the internal sphincter. In addition, half
of them extend out as far as the intersphincteric plane. Parks
first addressed their role in the pathogenesis of anorectal
abscesses and fistulas [7]. Immunochemical staining methods
have confirmed the presence of mucous secreting cells as well
as intraluminal secretions within the glands. It is controversial
whether these glands have a definite active secretory function
such as lubricating stool as it passes through the anal canal,
or merely are static outgrowths of the anal crypts that can
potentially become blocked with debris. Regardless, it seems
logical that an obstructed gland extending into the intershincteric space can develop into an abscess that can track along
or through adjacent tissue planes and upon spontaneous or
surgical drainage develop into a fistula. This concept is substantiated clinically since most internal fistulous openings
are found within the crypts at the dentate line.

9

Fig. 2.5 Illustration of Goodsall’s rule

The majority of the anal glands are located in the posterior
midline, which explains the prevalence of anorectal abscesses
in this region. When these posterior midline abcesses erode
into the adjacent deep postanal space, the septic process
gains access to the left and right ischiorectal spaces to form
a horseshoe abscess/fistula. The high concentration of anal
glands in this region helps explain Goodsall’s rule, which is
often useful in identifying the primary opening of a fistula
(Fig. 2.5). This guideline states that if the secondary opening

is situated around the posterior half of the anus or more than
3 cm away from the anus, the primary opening will usually
be located at the posterior midline. Conversely, if the secondary opening is found within the anterior half of the anus, the
internal opening will be directly in line (radially located) with
the secondary opening at the dentate line. However, there is
evidence suggesting that Goodsall’s rule is less accurate for
identifying fistulas with an anterior external opening [8].

Sphincter Architecture Based on Refined
Imaging Techniques
Traditional descriptions of sphincter architecture were based
on anatomic dissections and operative observations. With the
advent of endoanal ultrasound, in vivo evaluation of anal
anatomy and pathology became available. However, the
shortcoming of this technique was suboptimal delineation
of the external sphincter and levator ani muscles. Highspatial-resolution endoanal MR imaging using a coil affords
excellent resolution of all of the sphincter muscles. By utilizing this technique, normal sphincter anatomy in both men
and women was definitively presented. Among the major
findings in this study were that the anterior part of the external sphincter was about half as long in women compared
with men (14.0 mm vs. 27.0 mm). The thickness of each
sphincter component was roughly equivalent between the
sexes, and that there was a substantial difference in the
arrangement of muscle fibers anterior to the sphincter. In men
the central perineal tendon is a strong insertion point directly


10

R.K. Pearl

anterior to the external sphincter, whereas in women it is a
less well-defined insertion area of woven muscle fibers
slightly superior to the external sphincter. The significance
of this finding is that during vaginal delivery this tissue
becomes markedly attenuated predisposing it to obstetrical
tears which can clearly impact fecal continence. This anatomic arrangement in women along with the fact that the
puborectalis muscle is absent anteriorly should alert the surgeon to exercise caution when encountering an anterior fistula tract. Unless the fistula is extremely superficial, primary
fistulotomy should probably be avoided.

The Geography of the Anorectal Spaces
There are several spaces and potential spaces surrounding
the rectum and anal canal that are of surgical significance
(Fig. 2.6). The ischiorectal fossa is divided into the perianal
space and ischioanal space. The perianal space surrounds
the lowest portion of the anal canal and is confined by the
radiating elastic septae of the conjoined longitudinal muscle
attachments to the anoderm and perianal skin and contains
finely lobulated fat, delicate branches of hemorrhoidal vessels,
nerves, and lymphatics. When blood or pus accumulates in
this closed space the stretching and irritation of the many
nerve endings results in the severe anal pain associated with
perianal abscesses and thrombosed external hemorrhoids.
The ischioanal fossa surrounds the upper portion of the
anal canal to the level of the anorectal ring. The roof of this
pyramid-shaped space is composed of the levator ani muscles, and laterally it is bounded by the obturator internus
muscle which lines the pelvic sidewalls. It is filled with
coarsely lobulated fat and contains the inferior rectal vessels
and nerves. It is a relatively large space and can harbor a
substantial abscess with only minimal involvement of the
overlying gluteal skin. These clinical findings can mislead an

Fig. 2.6 Mid-sagittal view of the lower rectum and anal canal emphasizing the anorectal spaces

Fig. 2.7 Partial oblique view of the pelvic floor and anal sphincter
muscles from below. The arrow illustrates how the deep postanal space
serves as a window to the left and right ischiorectal spaces, which is
how horseshoe abscess/fistula forms. The location and course of the
inferior rectal nerves are shown to emphasize how they can be readily
avulsed by overaggressive spreading of curved clamps during drainage
of ischiorectal abscesses

inexperienced clinician into making the diagnosis of celluitis
rather than a drainable abscess with disastrous results especially in the case of a diabetic of immunocompromised
patient. The abscess cavity may extend around one-half the
circumference of the anus (horseshoe) or extend completely
around the anus (floating freestanding anus).
Another pitfall that sometimes occurs when draining a
large ischiorectal abscess is inadvertently mistaking the
fanned out array of branches of the inferior rectal nerve as
“loculations” inhibiting adequate drainage. Tearing these
branches by recklessly spreading a large curved clamp can
result in significant injury to the nerve supply to the external
sphincter. If this procedure is carried out on both sides as in
the case of a horseshoe abscess, complete denervation of the
sphincter can occur.
The superficial postanal space is located in the posterior
midline between the skin and anococcygeal ligament and is
frequently involved with anorectal abscesses. The deep postanal space (retrosphincteric space of Courtney) located deep
to the anococcygeal ligament and the upper portions of the
external sphincter and levator muscles is of special surgical

significance first because of the frequency of abscesses
occurring in this region, and secondly because the deep
postanal space serves as a window to the left and right ischiorectal spaces which can result in horseshoe abscesses or
fistulas (Fig. 2.7).
In longstanding horseshoe fistulas, the deep postanal
space can become quite indurated and rigid. Attempts to
sterilize and completely fill this infected cavity with collagen


2

11

Applied Anatomy

plugs or fibrin glue often fail because residual contaminated
space is left behind to reactivate the septic process.
The supralevator space is sandwiched between the upper
surface of the levators and pelvic peritoneum. Abscess
presenting in this location may be difficult to diagnose
especially when there are no visible clinical findings around
the perineum. Approximately 9 % of large ischiorectal
abscesses have an associated supralevator component,
which resulted from the septic process eroding through the
adjacent levator ani muscle resulting in an hourglass-shaped
abscess [9, 10].

AIDS have chronic diarrhea, which further exacerbates
the problem.
5. The presence of a high fistula in a patient with Crohn’s

disease. In these instances, it is prudent to mark the fistula
tract with a long-term seton such as a silastic vessel loop to
promote drainage and deter the development of recurrent
abscesses.
6. A marking seton should be placed whenever there is a
reasonable clinical suspicion that primary fistulotomy
will disrupt fecal continence.

Summary
When to Avoid Primary Fistulotomy
Anorectal examination under anesthesia is an important step
to assess the location and extent of the abscess/fistula process, as well as a means to determine how much sphincter
muscle is encircled by the tract. There are several circumstances where these findings can be particularly helpful in
preventing overly aggressive fistulotomy which may result in
fecal incontinence. In each of the following cases complete
primary fistulotomy should be avoided and be replaced by
more conservative procedures such as the judicious use of
setons, fistula plugs, fibrin glue, or eventually mucosal or
cutaneous advancement flap procedures:
1. The presence of a high transsphincteric fistula which can
be defined as involving more than 50 % of the external
sphincter posteriorly or laterally or 30 % of the external
sphincter anteriorly.
2. A transsphincteric fistula in cases of massive anorectal
sepsis (floating, freestanding anus) where the normal anatomic landmarks have been severely distorted such that
primary fistulotomy may compromise proper wound
healing resulting in a large gap or step-off deformity.
3. The existence of an anterior, high transsphincteric fistula
in a woman. The external sphincter is quite tenuous and
the puborectalis is absent in this region. Primary fistulotomy may result in fecal incontinence.

4. The presence of a high transsphincteric fistula in a patient
with poorly controlled acquired immunodeficiency syndrome (AIDS). Healing of anorectal wounds is notoriously
poor in these individuals. Moreover, many patients with

•
•
•
•

Anatomic considerations relating to fistula surgery
Sphincter architecture based on refined imaging techniques
Geography of the anal glands and anorectal spaces
When to avoid primary fistulotomy

References
1. Dalley AF. The riddle of the sphincters, the morphophysiology of
the anorectal mechanism reviewed. Am Surg. 1987;53:298–306.
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and colon. 5th ed. London: Balliere-Tindall; 1984.
3. Shafik A. A new concept of the anatomy of the anal sphincter mechanism and the physiology of defecation. The external anal sphincter: a triple-loop system. Invest Urol. 1975;12:412–9.
4. Rociu E, Stoker J, Eiijkemans MJC, Lameris JS. Normal anal
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spatial-resolution endoanal MR imaging. Radiology. 2000;
217:395–401.
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8. Cirocco WC, Reilly JC. Challenging the predictive accuracy of
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